Student: P.Umapathisivan Group 7 4TH Year 2nd sem K.S.M.

Cor Pulmonale
Cor pulmonale is defined as an alteration in the structure and

function of the right ventricle caused by a primary disorder of the respiratory system.Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur Pulmonary heart disease is enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs (pulmonary hypertension Producing pulmonary artery hypertension that may be due to intrinsic pulmonary disease an abnormal chest bellows, or a depressed ventilatory drive)

Classification
Accute {cause by pulmonary embolism (more

common) and acute respiratory distress syndrome (ARDS)} Chronic(cause by chronic respratory disease )

Etiology of Cor Pulmonale ( I )

Lung and Airways
COPD Asthma Bronchiectasis DILD Pulmonary

tuberculosis

Vascular Occlusion Multiple Emboli Schistosomiasis Filariasis Sickle Cell P. Pulmonary Hypertension

Etiology of Cor Pulmonale ( II )

Thoracic Cage Kyphosis > 100 o Scoliosis > 120 o Thoracoplasty Pleural fibrosis N-M Disease Polio Myelitis Myasthenia Gravis ALS Muscular Dystrophy

Etiology of Cor Pulmonale ( III )

Abnormal Respiratory Control Idiopathic hypoventilation Syndrome Obesity hypoventilation syndrome (Pick-Wickian syndrome) Cerebrovascular disease

Pathogenesis

 alterations in pulmonary circulation lead to pulmonary arterial hypertension and an

increased mechanical load on RightVentricle emptying (afterload) Pulmonary hypertension can be caused by irreversible reduction in the size of the vascular bed, as in diseases primarily affecting pulmonary blood vessels

Hypercapnea

Chronic lung disease

Anatomic changes

Acidemia

Hypoxia

Pulmonary Vessel Restriction

Increased Viscosity
Acidosis

Increased C.O.

Chronic Cor Pulmonale Rt. Ventricular Failure

Symptoms
Exertional dyspnea Syncopal attacks on exertion

substernal anginal
fatigue on exertion Shortness of breath which occurs on exertion but

when severe can occur at rest Wheezing Chronic wet cough Drop of systemic pressure Bluish discoloration of face

Signs
left parasternal systolic lift loud pulmonic 2nd sound pulmonary hypertension right ventricular hypertrophy (RVH) RV failure An increase in chest diameter labored respiratory efforts with retractions of the chest

wall distended neck veins with prominent a or v waves cyanosis may be seen.

Physical examination
Physical findings vary according to the underlying conditions that produced

CP. Tachypnea, cyanosis, elevated jugular venous pressure, a right ventricular parasternal impulse, hepatomegaly, and peripheral edema often are noted, particularly in patients with right ventricular failure. Physical findings in CP 1 are: Tachypnea Cyanosis Clubbing Elevated jugular venous pressure, often with a prominent atrial (a) wave Abnormalities of the chest or lungs depending on underlying condition causing cor pulmonale Soft or inaudible heart sounds Right ventricular impulse palpated along left sternal border or in epigastrium Right ventricular S3 or S4 (or both) Murmur of tricuspid insufficiency Hepatomegaly Ascites Peripheral edema

Diagnosis
In many cases, the diagnosis of pulmonary heart

disease is not easy as both the lung and heart disease can produce similar symptoms. Most patients undergo an ECG, chest X ray,echocardiogram, CT scan of the chest and a cardiac catheterization.

Auscultation of the lung

wheezes and crackles may be heard as signs of

underlying lung disease. Turbulent flow through recanalized vessels in chronic thromboembolic pulmonary hypertension may be heard as systolic bruits in the lungs.

Auscultation of the Heart

Splitting of the second heart sound with accentuation

of the pulmonic component can be heard in early stages. A systolic ejection murmur with sharp ejection click over the region of the pulmonary artery may be heard in advanced disease, along with a diastolic pulmonary regurgitation murmur. Other findings upon auscultation of the cardiovascular system may be third and fourth sounds of the heart and systolic murmur of tricuspid regurgitation

ECG in Cor Pulmonale

Electrocardiographic (ECG) abnormalities in cor pulmonale

reflect the presence of right ventricular hypertrophy (RVH), RV strain, or underlying pulmonary disease (see the image below). Such ECG changes may include the following: Right axis deviation R/S amplitude ratio in V1 greater than 1 (an increase in anteriorly directed forces may be a sign of posterior infarction) R/S amplitude ratio in V6 less than 1 P-pulmonale pattern (an increase in P wave amplitude in leads 2, 3, and aVF) S1 Q3 T3 pattern and incomplete (or complete) right bundle branch block, especially if pulmonary embolism is the underlying etiology Low-voltage QRS because of underlying COPD with hyperinflation Severe RVH may reflect as Q waves in the precordial leads that may be mistakenly interpreted as an anterior myocardial infarction (however, as electrical activity of the RV is significantly less than the left ventricle [LV], small changes in RV forces may be lost in the ECG).

Chest X-ray
enlargement of the central pulmonary arteries with

oligemic peripheral lung fields Pulmonary hypertension should be suspected when the right descending pulmonary artery is larger than 16 mm in diameter and the left pulmonary artery is larger than 18 mm in diameter Right ventricular enlargement leads to an increase of the transverse diameter of the heart shadow to the right on the postero anterior view and filling of the retrosternal air space on the lateral view. These findings have reduced sensitivity in the presence of kyphoscoliosis or hyperinflated lungs.

2-D and Doppler Echocardiography

Two-dimensional (2-D) echocardiography usually demonstrates

signs of chronic right ventricular (RV) pressure overload. As this overload progresses, increased thickness of the RV wall with paradoxical motion of the interventricular septum during systole occurs. At an advanced stage, RV dilatation occurs, and the septum shows abnormal diastolic flattening. In extreme cases, the septum may actually bulge into the left ventricular (LV) cavity during diastole, resulting in decreased LV diastolic volume and reduction of LV output. Doppler echocardiography is used to estimate pulmonary arterial pressure, taking advantage of the functional tricuspid insufficiency that is usually present in pulmonary hypertension. This imaging modality is considered the most reliable noninvasive technique to estimate pulmonary artery pressure. However, the efficacy of Doppler echocardiography may be limited by the ability to identify an adequate tricuspid regurgitant jet, which may be further enhanced by using saline contrast.

Cardiac catheterization
During a cardiac catheterization, a small flexible tube

is inserted from the groin and under x ray guidance images of the heart are obtained. Moreover the technique allows measurement of pressures in the lung and heart which provide a clue to the diagnosis

Differential diagnosis
When diagnosing cor pulmonale, it is important to consider the possibility of thromboembolic disease and primary pulmonary hypertension as possible etiologies. In addition, also assess for the following conditions:

Atrial myxoma

Blood disorders that are associated with increased blood

viscosity Congestive (biventricular) heart failure Constrictive pericarditis High-output heart failure Infiltrative cardiomyopathies Primary pulmonic stenosis Right heart failure due to right ventricular infarction Right-sided heart failure due to congenital heart diseases Ventricular septal defect

Management
Treatment of the underlying pulmonary disease
Improving oxygenation Right Ventricular (RV) function by increasing RV

contractility and decreasing pulmonary vasoconstriction. the approach might be different to some degree in an acute setting, with priority given to stabilizing the patient.

Oxygen Therapy
Oxygen therapy is of great importance in patients with underlying COPD, particularly when administered on a continuous basis. With cor pulmonale, the partial pressure of oxygen (PaO2) is likely to be below 55 mmHg and decreases further with exercise and during sleep. Oxygen therapy relieves hypoxemic pulmonary vasoconstriction, which then improves cardiac output, lessens sympathetic vasoconstriction, alleviates tissue hypoxemia, and improves renal perfusion. The multicenter, randomized Nocturnal Oxygen Therapy Trial (NOTT) showed that continuous low-flow oxygen therapy for patients with severe COPD resulted in significant reduction in the mortality rate.[13] In general, in patients with COPD, long-term oxygen therapy is recommended

when the PaO2 is less than 55 mm Hg or the O2 saturation is less than 88%. However, in the presence of cor pulmonale or impaired mental or cognitive function, long-term oxygen therapy can be considered even if the PaO2 is greater than 55 mm Hg or the O2 saturation is greater than 88%. Although whether oxygen therapy improves survival in patients with cor pulmonale due to pulmonary disorders other than COPD is not clear, it may provide some degree of symptomatic relief and improvement in functional status. Therefore, oxygen therapy plays an important role in both the immediate setting and long-term management, especially in patients who are hypoxic and have COPD.

Pharmacotherapy
Diuretic agents Vasodilator drugs Beta-selective agonist drugs Cardiac glycoside agents Theophylline Warfarin bronchodilation and infection treatment in patients

with chronic obstructive pulmonary disease (COPD) steroid and immunosuppressive agents in infiltrative and fibrotic lung diseases

Surgical Management of Cor Pulmonale

Phlebotomy is indicated in patients with chronic cor

pulmonale and chronic hypoxia causing severe polycythemia Pulmonary embolectomy is efficacious for unresolved pulmonary emboli Single-lung, double-lung, and heart-lung transplantation are all used to salvage the terminal phases of several diseases

Complications
Syncope Hypoxia Pedal edema Passive hepatic congestion Death.

Prevention
Patient education regarding the importance of

adherence to medical therapy is vital, because appropriate treatment of both hypoxia and underlying medical illness can improve mortality and morbidity.

Prognosis of Cor Pulmonale

Development of cor pulmonale as a result of a primary

pulmonary disease usually heralds a poorer prognosis. For example, patients with chronic obstructive pulmonary disease (COPD) who develop cor pulmonale have a 30% chance of surviving 5 years. However, whether cor pulmonale carries an independent prognostic value or is simply reflecting the severity of underlying COPD or other pulmonary disease is not clear. following factors may be independent predictors of inhospital mortality Age older than 65 years Bed rest for longer than 72 hours Chronic cor pulmonale Sinus tachycardia Tachypnea